GALLIUM-ARSENIDE AUGMENTS ANTIGEN-PROCESSING BY PERITONEAL-MACROPHAGES FOR CD4(-CELL STIMULATION() HELPER T)

Citation
Cb. Hartmann et Kl. Mccoy, GALLIUM-ARSENIDE AUGMENTS ANTIGEN-PROCESSING BY PERITONEAL-MACROPHAGES FOR CD4(-CELL STIMULATION() HELPER T), Toxicology and applied pharmacology, 141(2), 1996, pp. 365-372
Citations number
39
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology
ISSN journal
0041008X
Volume
141
Issue
2
Year of publication
1996
Pages
365 - 372
Database
ISI
SICI code
0041-008X(1996)141:2<365:GAABP>2.0.ZU;2-G
Abstract
Gallium arsenide (GaAs) suppresses numerous immunologic functions of l eukocytes at distal locations from the exposure site. The effect of di rect GaAs exposure on peritoneal cells was examined by ip administrati on of the chemical. No alteration in the frequency of various cell lin eages, including macrophages, B cells, CD4(+) and CD8(+) T cells, and granulocytes, occurred within the peritoneal population from GaAs-expo sed mice. The ability of macrophages to function as antigen-presenting cells (APC) by processing a panel of soluble protein antigens was inv estigated by the stimulation of antigen-specific helper T cell hybrido mas to secrete interleukin-2. On a per cell basis, GaAs-exposed macrop hages were more efficient than vehicle control cells in activating the T cells with all native antigens examined. GaAs exposure increased th e expression of major histocompatibility complex class II molecules, w hich are recognized by these T cells, on the surface of macrophages. H owever, the level of T cell activation with peptide fragments of the a ntigens, which do not require processing, was not enhanced with GaAs-e xposed cells as APC. In contrast, the capability of latex bead-exposed macrophages to function as APC was comparable to that of vehicle cont rol cells, suggesting that GaAs modulatory effects were not merely due to phagocytosis of particles. These findings suggest that direct GaAs exposure augments antigen processing, but not presentation, by macrop hages perhaps by activating the cells, which may contribute to the imm unotoxicity and inflammatory reaction caused by respiratory exposure t o GaAs. (C) 1996 Academic Press, Inc.